CD27 is a member of the tumor necrosis factor receptor superfamily.[5] It is currently of interest to immunologists as a co-stimulatory immune checkpoint molecule, and is the target of an anti-cancer drug in clinical trials.[6]
During mouse embryonic development, specific (medium) expression levels of CD27 (in addition to high cKit,[7][8] medium Gata2,[9][10][8] and high CD31[8] expression levels) define the very first adult definitive hematopoietic stem cells generated in the aorta-gonad-mesonephros region.[8] Furthermore, CD27 is expressed on both naïve and activated effector T cells as well as NK cells and activated B cells.[5] It is a type I transmembrane protein with cysteine-rich domains, but once T cells have become activated, a soluble form of CD27 can be shed.[5][6]
The protein encoded by this gene is a member of the TNF-receptor superfamily.[11] This receptor is required for generation and long-term maintenance of T cell immunity. It binds to ligand CD70, and plays a key role in regulating B-cell activation and immunoglobulin synthesis.[5]
When CD27 binds CD70, a signaling cascade leads to the differentiation and clonal expansion of T cells.[11] The cascade also results in improved survival and memory of cytotoxic T cells and increased production of certain cytokines.[12] This receptor transduces signals that lead to the activation of NF-κB and MAPK8/JNK.[11] Adaptor proteins TRAF2, TRAF3, and TRAF5 have been shown to mediate the signaling process of this receptor via ubiquitination.[5][6] CD27-binding protein (SIVA), a proapoptotic protein, can bind to this receptor and is thought to play an important role in the apoptosis induced by this receptor.[13]
In murine γδ T cells its expression has been correlated with the secretion of IFNγ.[14]
Varlilumab is an IgG1 antibody that binds to CD27 and is an experimental cancer treatment.[6] This agonist antibody stimulates CD27 when it binds.[6] The drug is in early clinical trials and appears to stimulate T cells and increase production of cytokines such as interferon-gamma.[6][11]
CD27 has been shown to interact with SIVA1,[15] TRAF2[16][17] and TRAF3.[16][17]
Some mutations can decrease the expression of CD27. Three such mutations, C53Y, C96Y, and R107C, are located in the cysteine-rich domains of CD27.[5]
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Cluster of differentiation by lineage
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